Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
20
|
| pubmed:dateCreated |
1998-10-23
|
| pubmed:abstractText |
The lithium-pilocarpine model of status epilepticus (SE) was used to study the type and distribution of seizure-induced neuronal injury in the rat and its consequences during development. Cell death was evaluated in hematoxylin- and eosin-stained sections and by electron microscopy. Damage to the CA1 neurons was maximal in the 2- and 3-week-old pups and decreased as a function of age. On the other hand, damage to the hilar and CA3 neurons was minimal in the 2-week-old rat pups but reached an adult-like pattern in the 3-week-old animals, and damage to amygdalar neurons increased progressively with age. The 3-week-old animals also demonstrated vulnerability of the dentate granule cells. To evaluate neuronal apoptosis, we used terminal deoxynucleotidyl transferase-mediated biotinylated UTP nick end labeling (TUNEL) stain, confocal fluorescence microscopy of ethidium bromide-stained sections, electron microscopy, and DNA electrophoresis. Neurons displaying all of those features of apoptotic death in response to SE were seen in the CA1 region of the 2-week-old pups and in the hilar border of the dentate granule cells of the 3-week-old animals. Some (3/11) of the animals that underwent SE at 2 weeks of age and most of the animals that underwent SE at 3 or 4 weeks of age (8/11 and 6/8, respectively) developed spontaneous seizures later in life; the latter showed SE-induced synaptic reorganization as demonstrated by Timm methodology. These results provide strong evidence for the vulnerability of the immature brain to seizure-induced damage, which bears features of both necrotic and apoptotic death and contributes to synaptic reorganization and the development of chronic epilepsy.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Oct
|
| pubmed:issn |
0270-6474
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
15
|
| pubmed:volume |
18
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
8382-93
|
| pubmed:dateRevised |
2007-11-14
|
| pubmed:meshHeading |
pubmed-meshheading:9763481-Age Factors,
pubmed-meshheading:9763481-Animals,
pubmed-meshheading:9763481-Apoptosis,
pubmed-meshheading:9763481-Behavior, Animal,
pubmed-meshheading:9763481-DNA,
pubmed-meshheading:9763481-Electroencephalography,
pubmed-meshheading:9763481-Female,
pubmed-meshheading:9763481-In Situ Nick-End Labeling,
pubmed-meshheading:9763481-Lithium,
pubmed-meshheading:9763481-Male,
pubmed-meshheading:9763481-Microscopy, Electron,
pubmed-meshheading:9763481-Mossy Fibers, Hippocampal,
pubmed-meshheading:9763481-Muscarinic Agonists,
pubmed-meshheading:9763481-Neuronal Plasticity,
pubmed-meshheading:9763481-Neurons,
pubmed-meshheading:9763481-Pilocarpine,
pubmed-meshheading:9763481-Rats,
pubmed-meshheading:9763481-Rats, Wistar,
pubmed-meshheading:9763481-Status Epilepticus,
pubmed-meshheading:9763481-Synapses
|
| pubmed:year |
1998
|
| pubmed:articleTitle |
Patterns of status epilepticus-induced neuronal injury during development and long-term consequences.
|
| pubmed:affiliation |
Department of Neurology, University of California Los Angeles School of Medicine, Los Angeles, California 90095-1752, USA.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.
|